A 42-year-old woman with witnessed out-of-hospital cardiac arrest (CA) reached the emergency department after 38 minutes of cardiopulmonary resuscitation. Since the return of spontaneous circulation did not occur, extracorporeal membrane oxygenation (ECMO) was applied. The ECMO circuit was connected to a heat exchanger to induce therapeutic hypothermia (34°C). Continuous EEG monitoring with a simplified 4-channel montage (EEG Infinity POD, Dräger, Lübeck, Germany) was started. After 24 hours of hypothermia, the patient was gradually rewarmed, according to the local protocol. At the withdrawal of sedation, she remained comatose, and standard reduced-montage (8-channel) EEG showed nonconvulsive status epilepticus (NCSE, figure e-1 at Neurology.org/cp), which was initially treated with propofol and valproate infusion (20 mg/kg followed by 1 mg/kg/hr). She was weaned from ECMO 48 hours after CA. She remained in a coma, all brainstem reflexes were present, neuron-specific enolase was 21 ng/mL, and brain CT scan was normal, with no evidence of traumatic brain injury or other brain lesions. Standard EEG was repeated and showed refractory NCSE. Levetiracetam was added (2,000 mg bolus followed by 2,000 mg/24 hours), and propofol-induced coma was initiated to obtain a burst-suppression pattern for 24 hours, guided by EEG monitor. Propofol was gradually stopped 72 hours after CA, and EEG still showed refractory NCSE. High-dose barbiturate coma was induced (thiopental 10 mg/kg/hr). At this time point, EEG was isoelectric and the patient was hemodynamically stable. Median nerve somatosensory evoked potentials (SSEP, see figure 1 for technical details) were recorded 72 hours after CA, and N20 cortical responses were bilaterally absent, while potentials at Erb point (N9), cervical spine (N13), and lower brainstem (P14) were present (figure 1A). Barbiturate coma was maintained for 24 hours. After barbiturate withdrawal, EEG showed diffuse slow wave activity with superimposed irregular beta activity. SSEP recording was repeated 10 days after the first recording (9 days after thiopental withdrawal) and showed bilateral reappearance of the N20 response (figure 1B). The patient showed a gradual improvement in both consciousness and neurologic examination and was discharged from the intensive care unit 4 weeks after CA. At 3-month follow-up she was independent in activities of daily living (Cerebral Performance Category 2).

Coppo, A., Beretta, S., Migliari, M., Ferrarese, C., Avalli, L. (2015). Absence and reappearance of N20 response after thiopental withdrawal in postanoxic coma. NEUROLOGY. CLINICAL PRACTICE, 5(6), 488-490 [10.1212/CPJ.0000000000000135].

Absence and reappearance of N20 response after thiopental withdrawal in postanoxic coma

Coppo A.;Beretta S.;Migliari M.;Ferrarese C.;Avalli L.
2015

Abstract

A 42-year-old woman with witnessed out-of-hospital cardiac arrest (CA) reached the emergency department after 38 minutes of cardiopulmonary resuscitation. Since the return of spontaneous circulation did not occur, extracorporeal membrane oxygenation (ECMO) was applied. The ECMO circuit was connected to a heat exchanger to induce therapeutic hypothermia (34°C). Continuous EEG monitoring with a simplified 4-channel montage (EEG Infinity POD, Dräger, Lübeck, Germany) was started. After 24 hours of hypothermia, the patient was gradually rewarmed, according to the local protocol. At the withdrawal of sedation, she remained comatose, and standard reduced-montage (8-channel) EEG showed nonconvulsive status epilepticus (NCSE, figure e-1 at Neurology.org/cp), which was initially treated with propofol and valproate infusion (20 mg/kg followed by 1 mg/kg/hr). She was weaned from ECMO 48 hours after CA. She remained in a coma, all brainstem reflexes were present, neuron-specific enolase was 21 ng/mL, and brain CT scan was normal, with no evidence of traumatic brain injury or other brain lesions. Standard EEG was repeated and showed refractory NCSE. Levetiracetam was added (2,000 mg bolus followed by 2,000 mg/24 hours), and propofol-induced coma was initiated to obtain a burst-suppression pattern for 24 hours, guided by EEG monitor. Propofol was gradually stopped 72 hours after CA, and EEG still showed refractory NCSE. High-dose barbiturate coma was induced (thiopental 10 mg/kg/hr). At this time point, EEG was isoelectric and the patient was hemodynamically stable. Median nerve somatosensory evoked potentials (SSEP, see figure 1 for technical details) were recorded 72 hours after CA, and N20 cortical responses were bilaterally absent, while potentials at Erb point (N9), cervical spine (N13), and lower brainstem (P14) were present (figure 1A). Barbiturate coma was maintained for 24 hours. After barbiturate withdrawal, EEG showed diffuse slow wave activity with superimposed irregular beta activity. SSEP recording was repeated 10 days after the first recording (9 days after thiopental withdrawal) and showed bilateral reappearance of the N20 response (figure 1B). The patient showed a gradual improvement in both consciousness and neurologic examination and was discharged from the intensive care unit 4 weeks after CA. At 3-month follow-up she was independent in activities of daily living (Cerebral Performance Category 2).
Articolo in rivista - Articolo scientifico
etiracetam, propofol, thiopental, valproic acid
English
488
490
3
Coppo, A., Beretta, S., Migliari, M., Ferrarese, C., Avalli, L. (2015). Absence and reappearance of N20 response after thiopental withdrawal in postanoxic coma. NEUROLOGY. CLINICAL PRACTICE, 5(6), 488-490 [10.1212/CPJ.0000000000000135].
Coppo, A; Beretta, S; Migliari, M; Ferrarese, C; Avalli, L
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/279747
Citazioni
  • Scopus 0
  • ???jsp.display-item.citation.isi??? ND
Social impact